OBJECTIVE Spinal cord injury (SCI) is a neurological disease with high incidence and disability. In this paper, we made a foundational study in long non-coding RNA paternally expressed gene 10 (lncRNA PEG10) at PC-12 cells. METHODS We used CCK8, flow cytometry, migration and invasion assay to detect changes at the cellular level. PEG10, microRNA-34a-5p (miR-34a-5p) and TLX transfected by transfection assay and amplified by real-time quantitative PCR (qRT-PCR). TLX expression and proteins about apoptosis and pathways were investigated by Western blot. Additionally, the relationship between PEG10 and miR-34a-5p, miR-34a-5p and TLX were examined through luciferase assay. RESULTS H2O2-injury model was established. Knockdown PEG10 deteriorated H2O2-injury. miR-34a-5p was confirmed as a target of PEG10 and miR-34a-5p inhibitor remitted PEG10-induced H2O2-injury. Moreover, TLX was confirmed as a target miR-34a-5p and TLX remitted H2O2-injury. At last, TLX worked in H2O2-injury via Smad and Wnt/β-catenin pathways. CONCLUSION Knockdown PEG10 remitted H2O2-injury of PC-12 cells by targeting miR-34a-5p/TLX, and the behavior may be involved in Smad and Wnt/β-catenin pathways.

中文翻译：

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敲低 PEG10 通过靶向 miR-34a-5p/TLX 来恶化 PC-12 细胞的 H2O2 损伤。

目的 脊髓损伤（SCI）是一种高发病率和致残率的神经系统疾病。在本文中，我们在 PC-12 细胞中对长链非编码 RNA 父系表达基因 10 (lncRNA PEG10) 进行了基础研究。方法我们使用CCK8、流式细胞术、迁移和侵袭测定来检测细胞水平的变化。PEG10、microRNA-34a-5p (miR-34a-5p) 和 TLX 通过转染试验转染并通过实时定量 PCR (qRT-PCR) 扩增。通过蛋白质印迹研究TLX表达和关于细胞凋亡和途径的蛋白质。此外，通过荧光素酶测定法检测了 PEG10 与 miR-34a-5p、miR-34a-5p 和 TLX 之间的关系。结果建立了H2O2损伤模型。击倒 PEG10 恶化了 H2O2 损伤。miR-34a-5p 被证实是 PEG10 的靶标，miR-34a-5p 抑制剂缓解了 PEG10 诱导的 H2O2 损伤。此外，TLX 被确认为靶 miR-34a-5p 并且 TLX 缓解了 H2O2 损伤。最后，TLX 通过 Smad 和 Wnt/β-catenin 通路在 H2O2 损伤中起作用。结论敲低PEG10通过靶向miR-34a-5p/TLX缓解H2O2对PC-12细胞的损伤，该行为可能参与Smad和Wnt/β-catenin通路。